Judith E. Allen

University of Manchester

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Dominik Rückerl

University of Manchester

Tara E. Sutherland

University of Aberdeen

Andrew S. MacDonald

University of Edinburgh

Rick M. Maizels

University of Glasgow

P’ng Loke

National Institute of Allergy and Infectious Diseases

Stephen J. Jenkins

University of Edinburgh

Brian H. K. Chan

University of Manchester

Andrea L. Graham

Princeton University

James E Parkinson

University of Manchester

Matthew D. Taylor

New South Wales Department of Primary Industries

Cooperative Institutions

University of Edinburgh

199

Centre National pour la Recherche Scientifique et Technique (CNRST)

152

University of Manchester

139

Manchester Academic Health Science Centre

103

Commissariat à l'Énergie Atomique et aux Énergies Alternatives

Illinois Institute of Technology

IIT Research Institute

Laboratoire de Chimie

Centre for Inflammation Research

Centre for Immunity, Infection and Evolution

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Inflammasome-Independent Role for NLRP3 in Controlling Innate Antihelminth Immunity and Tissue Repair in the Lung

The Journal of Immunology (2019)

Alistair Chenery Rafid Al-Hallaf Zainab Agha Jesuthas Ajendra James E Parkinson

Abstract Alternatively activated macrophages are essential effector cells during type 2 immunity and tissue repair following helminth infections. We previously showed that Ym1, an alternative activation marker, can drive innate IL-1R–dependent neutrophil recruitment during infection with the lung-migrating nematode, Nippostrongylus brasiliensis, suggesting a potential role for the inflammasome in the IL-1–mediated innate response to infection. Although inflammasome proteins such as NLRP3 have important proinflammatory functions in macrophages, their role during type 2 responses and repair are less defined. We therefore infected Nlrp3−/− mice with N. brasiliensis. Unexpectedly, compared with wild-type (WT) mice, infected Nlrp3−/− mice had increased neutrophilia and eosinophilia, correlating with enhanced worm killing but at the expense of increased tissue damage and delayed lung repair. Transcriptional profiling showed that infected Nlrp3−/− mice exhibited elevated type 2 gene expression compared with WT mice. Notably, inflammasome activation was not evident early postinfection with N. brasiliensis, and in contrast to Nlrp3−/− mice, antihelminth responses were unaffected in caspase-1/11–deficient or WT mice treated with the NLRP3-specific inhibitor MCC950. Together these data suggest that NLRP3 has a role in constraining lung neutrophilia, helminth killing, and type 2 immune responses in an inflammasome-independent manner.

10.4049/jimmunol.1900640

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Citations (28)

Evolutionary Causes and Consequences of Immunopathology

Annual Review of Ecology Evolution and Systematics (2005)

Andrea L. Graham Judith E. Allen Andrew F. Read

▪ Abstract Immune responses can cause severe disease, despite the role immunity plays in defending against parasitism. Indeed, immunopathology is a remarkably common cause of disease and has strong impacts upon both host and parasite fitness. Why has immune-mediated disease not been eliminated by natural selection? What constraints might immunopathology impose upon the evolution of resistance? In this review, we explore two major mechanistic causes of immunopathology in mammals and consider how such disease may have influenced immune system design. We then propose hypotheses that could explain the failure of natural selection to eliminate immunopathology. Finally, we suggest how the evolution of strategies for parasite virulence and host resistance may be shaped by this “double-edged sword” of immunity. Future work may reveal whether immunopathology constrains the evolution of resistance in all host taxa.

10.1146/annurev.ecolsys.36.102003.152622

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Citations (416)

Dietary protein supplementation results in molecular and cellular changes related to T helper type 2 immunity in the lung and small intestine in lactating rats re-infected with Nippostrongylus brasiliensis

Parasitology (2021)

Aya Masuda Judith E. Allen J.G.M. Houdijk Spiridoula Athanasiadou

Abstract Acquired immunity to gastrointestinal nematodes reduces during late pregnancy and lactation which is known as periparturient relaxation of immunity (PPRI). Protein supplementation reduces the degree of PPRI in a rat model re-infected with Nippostrongylus brasiliensis , but the underlying molecular mechanisms have yet to be elucidated. Here, we hypothesized that protein supplementation will enhance T helper type 2 immunity (Th2) in the lung and small intestine. Nulliparous Sprague-Dawley rats were given a primary infection of N. brasiliensis prior to mating and restrictedly fed diets with either low protein (LP) or high protein (HP) during pregnancy and lactation. Dams were secondary infected with N. brasiliensis on day 2 post-parturition, and histology and gene expression were analysed for tissue samples collected at days 5, 8 and 11. Genes related to Th2 immunity in the lung, Retnla , Il13 and Mmp12 , and in the intestine, Retnlb , were upregulated in HP dams compared to LP dams, which indicates the effect of dietary protein on Th2 immunity. HP dams also had increased splenic CD68 + macrophage populations compared to LP dams following secondary infection, suggesting enhanced immunity at a cellular level. Our data assist to define strategic utilization of nutrient supply in mammals undergoing reproductive and lactational efforts.

Nippostrongylus brasiliensis

Humoral immunity

Cellular immunity

10.1017/s0031182021001876

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Citations (1)

Deletion of Parasite Immune Modulatory Sequences Combined with Immune Activating Signals Enhances Vaccine Mediated Protection against Filarial Nematodes

PLoS neglected tropical diseases (2012)

Simon A. Babayan Honglin Luo Nicholas A. Gray David W. Taylor Judith E. Allen

Background Filarial nematodes are tissue-dwelling parasites that can be killed by Th2-driven immune effectors, but that have evolved to withstand immune attack and establish chronic infections by suppressing host immunity. As a consequence, the efficacy of a vaccine against filariasis may depend on its capacity to counter parasite-driven immunomodulation. Methodology and Principal Findings We immunised mice with DNA plasmids expressing functionally-inactivated forms of two immunomodulatory molecules expressed by the filarial parasite Litomosoides sigmodontis: the abundant larval transcript-1 (LsALT) and cysteine protease inhibitor-2 (LsCPI). The mutant proteins enhanced antibody and cytokine responses to live parasite challenge, and led to more leukocyte recruitment to the site of infection than their native forms. The immune response was further enhanced when the antigens were targeted to dendritic cells using a single chain Fv-αDEC205 antibody and co-administered with plasmids that enhance T helper 2 immunity (IL-4) and antigen-presenting cell recruitment (Flt3L, MIP-1α). Mice immunised simultaneously against the mutated forms of LsALT and LsCPI eliminated adult parasites faster and consistently reduced peripheral microfilaraemia. A multifactorial analysis of the immune response revealed that protection was strongly correlated with the production of parasite-specific IgG1 and with the numbers of leukocytes present at the site of infection. Conclusions We have developed a successful strategy for DNA vaccination against a nematode infection that specifically targets parasite-driven immunosuppression while simultaneously enhancing Th2 immune responses and parasite antigen presentation by dendritic cells.

Brugia malayi

10.1371/journal.pntd.0001968

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Citations (26)

Most of the Response Elicited againstWolbachiaSurface Protein in Filarial Nematode Infection Is Due to the Infective Larval Stage

The Journal of Infectious Diseases (2004)

Tracey J. Lamb Laëtitia Le Goff Agnes Kurniawan David B. Guiliano Katelyn Fenn

Immune responses to the intracellular Wolbachia bacteria of filarial nematodes are thought to contribute to the pathologic process of filarial infection. Here, we compare antibody responses of subjects living in an area where lymphatic filariasis is endemic with antibody responses elicited in a murine model of filarial infection, to provide evidence that the infective larval stage (L3), not adult nematodes, are the primary inducer of responses against Wolbachia. In human subjects, antibody responses to Brugia malayi Wolbachia surface protein (WSP) are most often correlated with antibody responses to the L3 stage of B. malayi. Analysis of anti-WSP responses induced in mice by different stages of the rodent filariae Litomosoides sigmodontis shows that the strongest anti-WSP response is elicited by the L3 stage. Although adult filarial nematode death may play a role in the generation of an anti-WSP response, it is the L3 stage that is the major source of immunogenic material, and incoming L3 provide a continual boosting of the anti-WSP response. Significant exposure to the endosymbiotic bacteria may occur earlier in nematode infection than previously thought, and the level of exposure to infective insect bites may be a key determinant of disease progression

Brugia malayi

Lymphatic Filariasis

Filarioidea

10.1086/380490

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Citations (27)

Th1-Th2: Reliable paradigm or dangerous dogma?

Immunology Today (1997)

Judith E. Allen Rick M. Maizels

Identification

Tribute

Paradigm shift

10.1016/s0167-5699(97)01102-x

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Citations (312)

Over expression of IL-10 by macrophages overcomes resistance to murine filariasis

Experimental Parasitology (2011)

Sabine Specht Matthew D. Taylor Marieke A. Hoeve Judith E. Allen Roland Lang

CD68

10.1016/j.exppara.2011.09.003

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Citations (14)

Additional file 10: of The IL-4/STAT6 signaling axis establishes a conserved microRNA signature in human and mouse macrophages regulating cell survival via miR-342-3p

Figshare (2016)

Zsolt Czimmerer Tamás Varga Máté Kiss Cesaré Vázquez Quang Doan-Xuan

List of miR-342-3p mimic-regulated genes in RAW264.7 mouse macrophages. (XLSX 472 kb)

Signature (topology)

STAT6

10.6084/m9.figshare.c.3643313_d1

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Citations (0)

LSC Abstract – Hookworm infection with nippostrongylus brasiliensis is a MyD88-TRIF independent mouse model of emphysema

Emma Ringqvist Tara E. Sutherland William Wallace Alison Fulton Sheelagh Duncan

Infections with the hookworm Nippostrongylus brasiliensis cause a rapid phase of pulmonary damage, immune activation, wound healing and then long term a progressive emphysematous pathology in mice. The emphysema is visible one month after the hookworm has left the lungs and was described but not further investigated in 2008. We characterized the immunological landscape from the infection, to investigate which cell types and activation pathways that are necessary for the emphysematous pathology by comparing BALB/c, C57BL/6 mice, IL-4Rα^-/- and MyD88-TRIF^-/- mice in time courses and long term. We could establish that the immunological activation published for day 42 post infection in BALB/c mice, reduce over time and is genotype specific. At two months post infection, only BALB/c mice had some immune activation in macrophage related transcripts Arg1 and IL-18. We could detect strong differences in neutrophil recruitment and macrophage activation between the four tested genotypes during the time course. Importantly, however, all of the genotypes had comparable emphysematous bullae and increased alveolar spaces. We have described that the progressive emphysematous pathology in this rodent infection model is not related to the tested immune parameters. Neither the strong neutrophilia, macrophage activation nor normal wound healing is necessary for developing the long term pathology. Importantly, there are no other mouse models that develop emphysema independently of MyD88 or TRIF signalling after injury or infection (ex. smoking, hypoxia). By further investigations, this model may give us useful insight into unidentified emphysema-driving molecular pathways. This abstract has been presented previously at the European Respiratory Society9s Lung Science Conference in March 2016.

Nippostrongylus brasiliensis

TRIF

10.1183/13993003.congress-2016.pa3413

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A Full Shift True Breathing Zone Air Sampler and Its Application to Lead Workers

Proceedings of the Institution of Mechanical Engineers (1981)

Judith E. Allen Edward G. Bellinger R I Higgins

A completely head-mounted full shift dust sampler for monitoring the lead-in-air concentration in a lead worker's actual breathing zone is described. A small filter head is positioned within 5 cm of the mouth and nose on an adjustable stalk. Air is drawn through a 1.25 cm diameter glass fibre filter at a rate of 0.51/min by a small rotary vane pump.Initial comparisons with a conventional lapel-mounted UKAEA head powered by a Casella pump show that the average lead-in air concentration in the true breathing zone can be significantly different from that around the lapel.

Lead (geology)

10.1243/pime_proc_1981_195_053_02

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Citations (2)